Publications
2000
Rihn B., Coulais C., Kauffer E., Bottin M. C., Martin P., Yvon F., Vigneron J. C., Binet S., Monhoven N., Steiblen G., Keith G.
Inhaled crocidolite mutagenicity in lung DNA Article de journal
Dans: Environ Health Perspect, vol. 108, no. 4, p. 341-6, 2000, (0091-6765 Journal Article).
Résumé | BibTeX | Étiquettes: &, Adducts/*genetics, Air, Alveolar/physiology, Animals, Asbestos, Crocidolite/administration, Damage/*genetics, DNA, dosage/*adverse, effects, effects/pathology, Exposure, Gov't, Inhalation, Lung/*drug, Macrophages, Male, Mice, Mutagenicity, Non-U.S., Pollutants/*adverse, Support, Tests, transgenic
@article{,
title = {Inhaled crocidolite mutagenicity in lung DNA},
author = { B. Rihn and C. Coulais and E. Kauffer and M. C. Bottin and P. Martin and F. Yvon and J. C. Vigneron and S. Binet and N. Monhoven and G. Steiblen and G. Keith},
year = {2000},
date = {2000-01-01},
journal = {Environ Health Perspect},
volume = {108},
number = {4},
pages = {341-6},
abstract = {We used transgenic mice carrying the lacI reporter gene to study the mutagenesis potential of asbestos crocidolite. The animals were exposed by nose-only inhalation to an aerosol containing 5.75 mg/m(3) crocidolite dust for 6 hr/day and 5 consecutive days. After 1, 4, and 12 weeks, we examined four end points: the cytology of bronchoalveolar lavage, the lung load of crocidolite, the hydrophobic DNA adducts, and the mutations in the lacI reporter gene. Twelve weeks after exposure, nearly 10% of the inhaled fibers remained in the lung (227 +/- 103 ng/mg lung). There was evidence of a typical inflammatory response consisting of multinucleate macrophages at weeks 4 and 12, whereas immediately after the exposure, we observed numerous polymorphonuclear neutrophils. The mutant frequency significatively increased during the fourth week after the exposure: 13.5 [time] 10(-5) in the exposed group versus 6. 9 10(-5) in the control group. The induction factor, defined by the ratio of checked mutants of exposed mice to checked mutants of control mice, was 1.96. The mutation spectrum of control lung DNA and exposed lung DNA was similar, suggesting the possible involvement of a DNA repair decrease in crocidolite-treated animals. We used the (32)P-postlabeling method and did not detect any increase of either 5 mC or bulky adduct in treated mice. This is the first study that demonstrates asbestos mutagenicity in vivo after a nose-only inhalation.},
note = {0091-6765
Journal Article},
keywords = {&, Adducts/*genetics, Air, Alveolar/physiology, Animals, Asbestos, Crocidolite/administration, Damage/*genetics, DNA, dosage/*adverse, effects, effects/pathology, Exposure, Gov't, Inhalation, Lung/*drug, Macrophages, Male, Mice, Mutagenicity, Non-U.S., Pollutants/*adverse, Support, Tests, transgenic},
pubstate = {published},
tppubtype = {article}
}
We used transgenic mice carrying the lacI reporter gene to study the mutagenesis potential of asbestos crocidolite. The animals were exposed by nose-only inhalation to an aerosol containing 5.75 mg/m(3) crocidolite dust for 6 hr/day and 5 consecutive days. After 1, 4, and 12 weeks, we examined four end points: the cytology of bronchoalveolar lavage, the lung load of crocidolite, the hydrophobic DNA adducts, and the mutations in the lacI reporter gene. Twelve weeks after exposure, nearly 10% of the inhaled fibers remained in the lung (227 +/- 103 ng/mg lung). There was evidence of a typical inflammatory response consisting of multinucleate macrophages at weeks 4 and 12, whereas immediately after the exposure, we observed numerous polymorphonuclear neutrophils. The mutant frequency significatively increased during the fourth week after the exposure: 13.5 [time] 10(-5) in the exposed group versus 6. 9 10(-5) in the control group. The induction factor, defined by the ratio of checked mutants of exposed mice to checked mutants of control mice, was 1.96. The mutation spectrum of control lung DNA and exposed lung DNA was similar, suggesting the possible involvement of a DNA repair decrease in crocidolite-treated animals. We used the (32)P-postlabeling method and did not detect any increase of either 5 mC or bulky adduct in treated mice. This is the first study that demonstrates asbestos mutagenicity in vivo after a nose-only inhalation.